运动疲劳大鼠丘脑腹外侧核神经元自发放电特征的分析

通过观察力竭运动对大鼠丘脑腹外侧核(VL)神经元自发放电活动的影响,探讨丘脑腹外侧核在运动疲劳中枢调控过程中的作用.选取雄性Wistar大鼠,随机分为对照组和疲劳组.采用跑台递增负荷运动方案,建立运动疲劳模型.采用玻璃微电极的体电生理学技术,观察丘脑腹外侧核神经元自发放电活动,并对其放电模式、放电频率、锋电位间隔直方图进行线下分析.得到了FG大鼠丘脑腹外侧核单簇发混合放电和规则单发放电神经元比例明显低于CG(P0.01),爆发式放电神经元比例明显高于CG(P0.01).FG大鼠丘脑腹外侧核神经元总放电频率显著低于CG(P0.05),规则单发放电频率有所升高,单簇发混合放电频率有所降低,但与CG相比均未见显著差异(P0.05).可以看出大鼠丘脑腹外侧核神经元参与了运动性疲劳的中枢调控.丘脑腹外侧核在运动疲劳引起间接通路与直接通路的调节功能失衡过程中起关键作用.     

电刺激岛叶对大鼠血压及缰核内神经元放电活动的影响

研究证明了缰核（Hb)是刺激岛叶（INS）所引起的升压效应下行通路的主要中继站之一。电刺激INS引起升压反应，在刺激电极的同侧Hb内微量注射盐酸利多卡因，电刺激INS所引起的升压反应降低了36.9%。双侧Hb内微量注射盐酸利多卡因，电刺激INS所引起的升压反应降低了41．7％。单侧或双侧Hb内微量注射生理盐水或人工脑脊液均不能降低电刺激INS所引起的升压反应。在刺激INS前后用微电极记录Hb内心血管调节相关神经元放电活动的变化。电刺激INS后，Hb内心血管调节相关神经元的放电频率明显增加者占58％（21／36），频率明显减少者占14％（5／36），频率无明显变化者占28％（10／36）。结论表明：缰核是参与电刺激岛叶引起升压效应的主要下行通路之一。     

Modulation of neuronal activity of cerebellar fastigial nucleus by locus coeruleus stimulation in the rat

The effects of stimulating locus coeruleus (LC) on neuronal activity of cerebellar fastigial nucleus (FN) was investigated. Stimulation of LC elicited inhibitory, excitatory and biphasic (inhibition-excitation) responses from FN cells. The majority of responsive cells showed an inhibitory response with a latency of less than 10 ms. Injection of α adrenoreceptor antagonists phentolamine (ⅳ) could block the inhibitory response of FN cells to the LC stimulation, but propranolol (ⅳ), a β adrenoreceptor antagonist, could not. These results suggest that LC-cerebellar noradrenergic afferent fibers may be involved in the cerebellar sensorimotor integration process by exerting their modulatory action on the cerebellar nuclear cells' activities.     

胰岛素及胰高血糖素对大白鼠缰核离体脑片神经元单位放电的影响

实验观察了胰岛素、胰血糖素及乙酰胆碱对离体脑片侧缰核神经元单位放电的作用,结果显示胰高血糖素和乙酰胆碱对内侧缰核神经元自发放电起兴奋作用,胰岛素起抑制作用。推测胰岛素和胰高血糖素对缰核神经元活动的影响,可能与参与应激性防御反应过程有关。     

电刺激大鼠mPFC对听皮层神经元听反应的影响

实验在40只成年SD大鼠上进行,使用常规电生理学方法,观察了电刺激大鼠内侧额叶前皮质(medial prefrontal cortex, mPFC)对听皮层神经元听反应的影响.在122个神经元上观察了电刺激mPFC对听反应的影响.对其中93个神经元作了详细分析发现,有73个神经元的听反应受到易化（39个,41.9%）或抑制（34个,36.6%）.刺激mPFC对听反应的影响存在最佳刺激间隔,大多数神经元（51个,69%）在10~15 ms之间.结果提示,大鼠mPFC可对听皮层神经元的听反应调制,这种调制可能是通过多级神经元环路实现的.     

β-Adrenergic activation enhances NMDA-induced current in pyramidal cells of the basolateral nucleus of amygdala

NMDA receptor （NMDA-R） in the amygdala complex is critical for both long-term potentiation （LTP） and formation of conditioned fear memory. It is reported that activation of β-adrenoceptors （β-AR） in the amygdala facilitates LTP and enhances memory consolidation. The present study examined the regulatory effect of β-AR activation on NMDA-R mediated current in pyramidal cells of the basolateral nucleus of amygdala （BLA）, using whole-cell recording technique. Bath application of the β-AR agonist isoproterenol enhanced NMDA-induced current, and this facilitatory effect was blocked by co-administered propranolol, a β-AR antagonist. The facilitatory effect of isoproterenol on NMDA-induced current could not be induced when the protein kinase A （PKA） inhibitor Rp-cAMPs was added in electrode internal solution.The present results suggest that β-AR activation in the BLA could modulate NMDA-R activity directly and positively, probably via PKA.     

Protein synthesis inhibition in the basolateral nucleus of amygdala facilitates extinction of auditory fear memory

It is known that consolidation of fear conditioning requires de novo protein synthesis in the amygdala. However, there is controversy about the role of protein synthesis in post-retrieval extinction of fear memory. The present study investigated the effect of protein synthesis inhibition (PSI) in the baso- lateral nucleus of amygdala (BLA) on post-retrieval extinction of auditory fear memory. Intra-BLA infu- sion of the protein synthesis inhibitor anisomycin ‘0’ h post-retrieval facilitated the extinction, but was ineffective if the memory was not retrieved. Anisomycin had no effect on the extinction when it was infused 6 h post-retrieval. The present results suggest that there exists a protein-synthesis-dependent mechanism in the BLA that retards extinction of auditory fear memory.     

刺激呈现率影响小鼠下丘神经元声反应特性

自由声场条件下,以强度为特征频率阈上5dBSPL、时程为40ms的短纯音为声刺激,记录了小鼠下丘神经元对不同呈现率（0．5～20Hz）的声刺激反应．结果显示,随呈现率的增高,绝大多数神经元（87．3％,103／118）的冲动发放数单调下降,少数（12．7％,15／118）神经元的冲动发放数呈非单调变化,冲动发放数与刺激呈现率之间有显著相关性．即使在低范围内改变呈现率也能显著影响多数神经元的声反应特性,其临界呈现率及最大呈现率低于3．3Hz的神经元分别超过70％（75．4％,89／118）和40％（44．9％,53／118）．此外,提高刺激呈现率,部分神经元（17．8％,21／118）的发放模式发生改变,主要是由紧张型或相位爆发型向相位型转变．可见,下丘神经元声反应特性与声刺激呈现率密切相关．     

电刺激小脑顶核对脑缺血再灌注氧化损伤作用的实验研究

探讨电刺激小脑顶核(FNs)对局部脑缺血再灌注氧化损伤作用的影响。以线性法制成大鼠右侧大脑中动脉缺血再灌注模型，随机分为假手术对照组、缺血再灌注(1／R)组、缺血再灌加电刺激小脑顶核组(1／R十FNs干预组)，免疫组化法检测诱生型环氧化酶(COX—2)表达，用硫代巴比妥酸法检测MDA含量。I／R组COX—2蛋白在半暗带呈强阳性表达，MDA含量明显升高，经电刺激小脑顶核后COX—2呈弱表达，MDA含量下降，有统计学差异。电刺激小脑顶核对脑缺血／再灌注后的氧化损伤具有拮抗作用。